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Biomedical subjects

J D Gillies

Publications and source records attributed to J D Gillies.

At least 19 recordsLinked to original sources
PubMed1981

Dose response of subcutaneous terbutaline and epinephrine in children with acute asthma.

In a double-blind dose response study in 26 children, 3, 6, or 12 microgram/kg of terbutaline sulfate was compared with 10 microgram/kg of epinephrine administered subcutaneously. In the first hour after injection, all doses of terbutaline and epinephrine resulted in improvement in mean clinical score, mean forced vital capacity, mean forced expiratory volume in the first second, and mean forced expiratory flow from 25% to 75% of vital capacity. Terbutaline epinephrine. However, while adverse effects following terbutaline were clinically imperceptible, epinephrine produced unpleasant headache and excitement in a few patients. Terbutaline did not change mean PaO2 or PaCO2 significantly in a subgroup of patients. The 12 microgram/kg dose of terbutaline was superior to 3 or 6 microgram/kg in relieving obstruction to airflow measured at the midportion of the vital capacity. This dose caused tremor in some children, but the tremor was not apparent to patients or their parents.

Adolescent↗
PubMed1980

Vegetative state following coma in childhood: evolution and outcome.

The data have been analysed for 17 children who showed features of the vegetative state following an acute illness that resulted in coma. 15 were under three years of age. Diffuse anoxia/ischaemia (N=12) and meningitis (N=4) were the most common causes of the comatose state. Seven children died, and nine of the 10 survivors have remained severely neurodevelopmentally handicapped, with no cognitive function (follow-up two months to five years). One child became ambulant a year after the initial insult and is moderately retarded. The findings suggest that children who develop the vegetative state following an illness resulting in coma have a poor prognosis and that decorticate or decerebrate responses, roving eye-movements and spontaneous blinking may be early indicators of its emergence.

Brain↗
PubMed1980

Radiologic assessment of severity of acute asthma in children.

In this prospective study, chest radiographs were obtained in 23 children during 33 acute asthmatic episodes. The degree of hyperinflation was assessed radiologically by three methods and compared to the clinical findings. There was no correlation between the radiologic impression of hyperinflation and the clinical severity of the asthmatic episode.

Adolescent↗
PubMed1979

Sural nerve effects on medial gastrocnemius motoneurones in the cat.

1. Excitability cycles for medial gastrocnemius motoneurones were recorded following sural nerve stimuli with amplitudes of 1.5, 3, 5, 10 and 40 times the nerve threshold. The monosynaptic reflex was time-integrated to quantify the motoneuronal output and some implications of this technique are discussed. In particular it is calculated that this method specifically examines the 15-25% most excitable motoneurones of the medial gastrocnemius pool.2. In most cases high amplitude stimulation of the sural nerve caused a triphasic (excitatory-inhibitory-excitatory) change in excitability. Arguments are given to support the conclusion that this represents a corresponding post-synaptic alteration in medial gastrocnemius motoneurone potential. It is concluded that this pattern illustrates the nature of the sural nerve projections to this portion of the medial gastrocnemius pool.3. The first period of excitation began after a latency, corrected to be compatible with intracellular recordings, of 2.8 ms and had a mean duration of 4.0 ms. The minimum stimulus level necessary for this effect lay between 1.5 and 3 times the nerve threshold. The maximum amplitude of this facilitation occurred with stimuli of 3-5 times threshold and was 60-90% of the amplitude of the monosynaptic facilitation which followed stimulation of the lateral gastrocnemius-soleus nerve.4. A period of inhibition followed immediately after the period of excitation and had a mean duration of 16 ms. The minimum stimulus level necessary for this effect lay between 1.5 and 3 times the nerve threshold and the degree of inhibition increased with stimuli up to 40 times threshold.5. The second period of excitation lasted a mean period of 50 ms and was due to activity in high threshold fibres. On average its amplitude was 50% that of the initial excitation.6. Exceptions to this triphasic variation of excitability were found. This result is interpreted as indicating the presence of projections with opposing actions which were simultaneously activated by sural stimuli.

Animals↗
PubMed1978

Radiologic findings in acute childhood asthma.

One hundred and seventy-eight admissions of 142 children with acute asthma were reviewed and graded for clinical severity. Abnormalities including consolidation (21%), atelectasis (3%) and pneumomediastinum (2%) were found on chest radiographs, most commonly in patients with clinically moderate or severe acute asthma. Hyperinflation proved difficult to assess, but was present in only 67% of admissions using the criteria described. The frequency of complications detected justifies the use of chest radiographs in assessing children admitted to hospital for acute asthma.

Adolescent↗
PubMed1977

Effects of neostigmine and pyridostigmine at the neuromuscular junction.

The effect of subcutaneous administration of pyridostigmine or neostigmine for 7 to 15 days on neuromuscular transmission has been studied in the rat phrenic nerve-hemidiaphragm preparation. The quantal contents of end-plate potentials at different stimulus rates and the amplitude and frequency of miniature end-plate potentials were compared with those of untreated controls. The rate of release of acetylcholine quanta at high stimulus rates, and the frequency of miniature end-plate potentials, were reduced by pretreatment with both pyridostigmine and neostigmine. Presynaptic effects differed in that the number of quanta released by each nerve impulse at a stimulus rate of 1/sec was not altered by pyridostigmine, but was reduced to 52% of normal by neostigmine. The amplitude of miniature end-plate potentials was reduced to 81% by pretreatment with neostigmine and to 54% by pretreatment with pyridostigmine. The cause appears to be a reduction in the number of acetylcholine receptor sites as a result of disorganisation of the postsynaptic muscle membrane, which may contribute to the muscular weakness associated with the long term use of anticholinesterase agents.

Animals↗
PubMed1976

The continual administration of neostigmine and the neuromuscular junction.

The effect of continual administration of neostigmine on the neuromuscular junction of the rat diaphragm was examined by determining the number of quanta of acetylcholine released by each nerve impulse, the effect of differing repetition rats on quantal release and the amplitude and frequency of miniature end-plate potentials. The number of quanta of acetylcholine released at a nerve impulse repetition rate of 1/sec was reduced to 51% of normal in treated animals. The reduction was greater at faster repetition rates. The amplitude of miniature end-plate potentials was reduced to 75% of normal. This reduction appears to be due to blocking of receptor sites rather than the reduction in the amount of acetylcholine in each quantum. The frequency of spontaneous miniature end-plate potentials was reduced in treated animals.

Acetylcholine↗
PubMed1971

Hamstrings stretch reflex in human spasticity.

In 16 patients with spastic paralysis the hamstrings stretch reflex was found to increase as the velocity of stretch increased, and generally to subside after movement ceased. These effects are attributable to the dynamic property of the primary spindle ending. The stretch reflex commonly appeared in only the last third of the stretching movement and was maximal as the knee became fully extended. This is consistent with the static properties of the primary and secondary spindle endings, and accounts for the absence of the clasp-knife phenomenon in the spastic hamstrings. The difference in the nature of the stretch reflex in spastic flexor and extensor muscles is best explained by the differential reflex effects of group II afferent fibres which facilitate flexor motoneurones and inhibit extensor motoneurones.

Electromyography↗